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Generation of aldehyde-derived protein modifications in ethanol-exposed heart
Onni Niemelä1, Seppo Parkkila, Simon Worrall
1Etela-Pohjanmaa Central Hospital Laboratory, Department of Clinical Chemistry and Institute of Medical Technology, University of Tampere, Finland. onni.niemela@epshp.fi
Background:
Although excessive ethanol consumption is known to lead to a variety of adverse effects in the heart, the molecular mechanisms of such effects have remained poorly defined. We hypothesized that posttranslational covalent binding of reactive molecular species to proteins occurs in the heart in response to acute ethanol exposure.
Methods:
The generation of protein adducts with several aldehydic species was examined by using monospecific antibodies against adducts with malondialdehyde (MDA), acetaldehyde (AA), MDA-AA hybrids, and hydroxyethyl radicals. Specimens of heart tissue were obtained from rats after intraperitoneal injections with alcohol (75 mmol/kg body weight) with or without pretreatment with cyanamide (0.05 mmol/kg body weight), an aldehyde dehydrogenase inhibitor.
Results:
The amounts of MDA and unreduced AA adducts were found to be significantly increased in the heart of the rats treated with ethanol, cyanamide, or both, whereas no other adducts were detected in statistically significant quantities. Immunohistochemical studies for characterization of adduct distribution revealed sarcolemmal adducts of both MDA and AA in the rats treated with ethanol and cyanamide in addition to intracellular adducts, which were also present in the group treated with ethanol alone.
Conclusions:
These findings support the role of enhanced lipid peroxidation and the generation of protein-aldehyde condensates in vivo as a result of excessive ethanol intake. These findings may have implications in the molecular mechanisms of cardiac dysfunction in alcoholics.
Insights
Excessive ethanol intake increases harmful protein adducts in the heart, specifically malondialdehyde (MDA) and acetaldehyde (AA) adducts. This suggests lipid peroxidation contributes to alcoholic heart dysfunction.
Area of Science:
- Cardiovascular Science
- Toxicology
- Biochemistry
Background:
- Molecular mechanisms of ethanol's cardiac effects are unclear.
- Excessive alcohol consumption damages the heart.
- Hypothesis: Ethanol exposure causes protein adducts in cardiac tissue.
Purpose of the Study:
- Investigate protein adduct formation in the heart after ethanol exposure.
- Examine the role of lipid peroxidation and aldehyde species.
Main Methods:
- Used antibodies to detect malondialdehyde (MDA) and acetaldehyde (AA) adducts.
- Analyzed rat heart tissue after ethanol and cyanamide (aldehyde dehydrogenase inhibitor) administration.
- Employed immunohistochemistry to map adduct distribution.
Main Results:
- Ethanol and cyanamide significantly increased MDA and AA adducts in rat hearts.
- Sarcolemmal and intracellular adducts were observed.
- No other adducts were detected in significant amounts.
Conclusions:
- Enhanced lipid peroxidation and protein-aldehyde condensate formation occur in vivo due to ethanol.
- These molecular changes may explain cardiac dysfunction in alcoholics.
